Abstract
Predominant Bcl-XL overexpression in pancreatic cancer cells blocks apoptosis, and may factor in chemoresistance. Bcl-XL depletion reverses this, enhancing chemotherapy-induced caspase activation, and TNF-alpha/TRAIL-induced apoptosis in vitro. We examined whether Bcl-XL depletion would alter tumor growth in vivo. Bcl-XL knockdown RNAi vectors were designed, constructed and introduced by retroviral infection into Panc-1 pancreatic cancer cells. A separate group of Panc-1 cells were similarly infected using a control RNAi vector.
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